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Inflammatory signaling refers to the complex network of biochemical pathways that coordinate the body's response to harmful stimuli, such as pathogens or tissue damage (Medzhitov, 2008). This process involves the activation of various pattern recognition receptors (PRRs) that trigger downstream cascades, including the NF-κB, MAPK, and JAK-STAT pathways (Newton & Dixit, 2012). These pathways lead to the production of pro-inflammatory mediators like cytokines (e.g., TNF-α, IL-6) and chemokines that orchestrate the immune response (Dinarello, 2018). While essential for host defense, dysregulated inflammatory signaling is a central feature of many chronic diseases, such as rheumatoid arthritis, inflammatory bowel disease, and atherosclerosis (Furman et al., 2019). Therapeutic strategies often involve targeting specific components of these pathways, such as using monoclonal antibodies to neutralize cytokines or small molecules to inhibit intracellular kinases (Schett et al., 2013).
Drugs modulate inflammatory signaling by inhibiting specific molecular components such as cytokines, cell surface receptors, or intracellular kinases to reduce the production and action of inflammatory mediators (Zarrin et al., 2021).
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